AI Article Synopsis
- The study analyzed gut mycobiomes in diabetic rats and compared them with normal rats over 4 months, confirming diabetes through high blood sugar levels.
- Changes in retinal tissues indicative of diabetic retinopathy were identified using histology and immunohistochemistry in diabetic rats.
- The gut mycobiomes showed significant dysbiosis in diabetic groups, with distinct clusters found through heat-map analysis, suggesting that increased pathogenic fungi may be linked to inflammation in diabetic rats.
Article Abstract
The current study compared the gut mycobiomes of diabetic rats generated by a streptozotocin chemical challenge, diabetic rats with retinal changes and normal control rats over a period of 4 months. Sustained increase in blood sugar levels (>150 mg/dL) confirmed the induction of diabetes. Histology and immunohistochemistry were used to identify changes in the retinal tissues in the diabetic rats indicative of the animals progressing into diabetic retinopathy. Gut mycobiomes generated using faecal DNA, indicated dysbiosis at the genus level in both diabetic (DM) and diabetic rats with retinal changes (DRC) when compared with the control rats. In Tables 3-6 the specific genera that were significantly increased/decreased in DM1 and DM2 and in DRC1 and DRC2 respectively compared to the respective controls CT1-CT4 rats are listed. Further, the mycobiomes of the DM and DRC rats separated into distinct clusters following heat-map analysis of the discriminating genera. In addition, β-diversity analysis separated the mycobiomes of DM and DRC rats from that of the control rats, but the mycobiomes of diabetic rats and diabetic rats with retinal changes showed an overlap. Based on the inferred functions of the discriminating genera in the mycobiomes, we speculated that increase in pathogenic fungi might contribute to the inflammatory status both in diabetic rats and rats showing retinal changes.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9017887 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0267080 | PLOS |
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